Neurochemicals

A mother’s care affects the infant’s hippocampus structure and function through epigenetic regulation of genes

gettingwell4 4-5 stars Advanced knowledge, Brain development, Epigenetics, Glutamate, Hippocampus, Limbic system, Memory, Neurochemicals, Stress

This 2012 McGill University rodent study found:

“Variations in maternal care in the rat affect hippocampal morphology and function as well as performance on hippocampal-dependent tests of learning and memory in the offspring.

Thus, in the rat, as in humans, social influences operate during early life to influence the structure and function of brain regions critical for cognitive capacity.

Variations in maternal care can influence hippocampal function and cognitive performance through the epigenetic regulation of genes.”

http://www.pnas.org/content/109/Supplement_2/17200.full “Variations in postnatal maternal care and the epigenetic regulation of metabotropic glutamate receptor 1 expression and hippocampal function in the rat”

The effects of early-life stress are permanent alterations in the child’s brain circuitry and function

gettingwell4 4-5 stars Advanced knowledge, Amygdala, Brain development, Cortisol, Limbic system, Memory, Neurochemicals, Stress ,

The sobering application of this 2013 rodent study’s finding was that if the limbic systems of human children weren’t already permanently damaged before they entered an orphanage, the orphanage experience would probably do that to them:

“The current study manipulates the type and timing of a stressor and the specific task and age of testing to parallel early-life stress in humans reared in orphanages.

The results provide evidence of both early and persistent alterations in amygdala circuitry and function following early-life stress.

These effects are not reversed when the stressor is removed nor diminished with the development of prefrontal regulation regions.”

http://www.pnas.org/content/110/45/18274.full “Early-life stress has persistent effects on amygdala function and development in mice and humans”

One way that mothers cause fear and emotional trauma in their infants

gettingwell4 4-5 stars Advanced knowledge, Amygdala, Brain development, Cortisol, Epigenetics, Limbic system, Memory, Neurochemicals, Stress , , ,

This 2014 rodent study showed that infants learned to fear specific items in the environment that their mothers feared. The imprinting memory happened at a stage in the infants’ lives when they hadn’t yet developed the physiology to respond to the environment with fear on their own.

The learning cue was the mothers’ fear response – in this case, her distress odor, even when the mother was not present – coupled with the infants’ stress. The fear memory was stored in the infants’ amygdalae:

“These memories are acquired at younger ages compared with amygdala-dependent odor-shock conditioning and are more enduring following minimal conditioning.

Our results provide clues to understanding transmission of specific fears across generations and its dependence upon maternal induction of pups’ stress response paired with the cue to induce amygdala-dependent learning plasticity.”

There’s no scientific reason why this and related studies shouldn’t inform researchers who ignore the earliest stages of human life when studying limbic system disorders in humans.

For an example of researchers choosing to NOT be informed, look at Is this science, or a PC agenda? Problematic research on childhood maltreatment and its effects.

http://www.pnas.org/content/111/33/12222.full “Intergenerational transmission of emotional trauma through amygdala-dependent mother-to-infant transfer of specific fear”

How painful long-lasting memories are stored and why they are so strong

gettingwell4 2-3 stars Required further work, Amygdala, Cortisol, Limbic system, Memory, Neurochemicals, Stress , ,

This 2014 rodent study provided evidence for a portion of the neurophysiology that underlies how painful long-lasting memories are stored and why they are so strong. The amygdala was the brain area studied.

The researchers were misguided in news coverage by focusing on solutions such as external mechanisms to forget these memories. The researchers should think in terms of how their research can help people who can help themselves instead of having something externally done to them.

After all, we’re humans who can participate in therapy, not lab rats who need to be fixed.

http://www.pnas.org/content/111/51/E5584.full “Hebbian and neuromodulatory mechanisms interact to trigger associative memory formation”

Are 50 Shades of Grey behaviors learned in infancy?

gettingwell4 5+ stars Premium, Amygdala, Brain development, Cerebrum, Cortisol, Epigenetics, Hypothalamus, Limbic system, Lower brain, Memory, Neurochemicals, Primal Therapy, Serotonin, Stress , , , , , ,

Ever wonder how someone could become attached to their early childhood abuser?

Ever wonder what underlying neurobiological conditions may account for the popularity of Fifty Shades of Grey?

This 2014 rodent study “Enduring good memories of infant trauma” linked below showed how trauma changed infants’ limbic system and lower brains. As adults, they derived a neurochemical benefit from re-experiencing the traumatic conditions:

“Trauma and pain experienced in infancy clearly led to higher rates of adult rat depression-like behavior..(but) the infant brain has limited ability to link trauma to fear areas in the brain, such as the amygdala.

These results are surprising because cues associated with trauma experienced as adults provoke fear and do not rescue depressive behavior.

It is possible that giving SSRI medications to children could be detrimental to mental health in adulthood,” Dr. Sullivan says. “We believe that our research offers the first evidence for the impact of serotonin pathways.

The infant trauma increases serotonin to produce brain programming of later life depression, and the infant trauma cue increases serotonin to alleviate the adult depressive like symptoms.”

As the study may apply to humans, let’s say that as an infant, someone was traumatized by a caregiver who, for example, bound them too tightly and left them alone for too long. What adult behaviors and other symptoms may develop as results? The person may:

  • Show depression-like symptoms that would strangely be alleviated by being bound tightly and left alone for an extended period.
  • Develop attachments to people who treated them poorly in a way that triggered them to re-experience their early childhood traumas.
  • Feel their mood lift when their infancy traumas were cued.
  • Be unable to explain and integrate with their cerebrum what was going on with their limbic system and lower brains.
  • Be caught in a circle of acting out their feelings and impulses, with unfulfilling results.

Isn’t it curious that this acting-out behavior – driven by unconscious memories of traumatic conditions – is a subject for popular entertainment? It may have resonated with personal experiences of the people who read the books and watched the movie.

What about people who want to be relieved of their symptomatic behavior? Is it a justifiable practice:

  • To pass affected people over to talk therapies that aren’t interested in directly treating the cause – a neurobiological condition that exists in the limbic system and lower brains – only the symptoms?
  • To drug affected people with the neurochemicals that their condition makes scarce – the symptoms – instead of addressing the source?

A principle of Dr. Arthur Janov’s Primal Therapy is that people are capable of treating their own originating neurobiological conditions. One of the therapeutic results is that the patient is relieved of being caught in endless circles of acting-out behavior.

That way we can have our own lives, and not be driven by what happened during early stages of our lives.

http://www.pnas.org/content/112/3/881.full “Enduring good memories of infant trauma: Rescue of adult neurobehavioral deficits via amygdala serotonin and corticosterone interaction”

Shorter telomere length in older men but not older women

gettingwell4 2-3 stars Required further work, Cortisol, Immune system, Neurochemicals, Stress, Telomeres

This 2014 UK human study was the first on telomere length I’ve curated, so here’s some background information:

“Telomeres are..structures..that cap the ends of..chromosomes, protecting them from end-to-end fusion and degradation during cell division.

Human telomeric DNA naturally shortens with age during..cell divisions and as a result of oxidative attack.

At critical shortness, telomeres exhibit impaired function, leading to genomic instability, apoptosis, and cell senescence, often with altered transcriptional programming and mitochondrial dysfunction.

In humans, mutations that directly compromise telomere maintenance cause premature mortality and onset of a spectrum of diseases overlapping with the age-related diseases common in the population.

Shorter telomere length in white blood cells is linked and, in some cases, anticipates aging-related morbidity and mortality from conditions with immune system involvement, such as infectious diseases, cancer, and cardiovascular diseases, as well as risk factors, including hypertension, diabetes, obesity, and smoking.

A critical determinant of telomere length is the enzyme telomerase, which has the capacity to add..onto the..ends of telomeric DNA, extending telomere length and promoting genomic stability.

Acute mental stress appears to increase telomerase enzymatic activity at least transiently, and it has been suggested that high telomerase activity in conjunction with shorter telomere length may be indicative of a stressed system.”

The study put UK civil service men and women ages 54 through 76 through a series of stress tests. They found that men with longer telomeres had quicker recovery times than did men with shorter telomeres.

Men with shorter telomeres and low telomerase activity also had quicker recovery times than did men with shorter telomeres and high telomerase activity:

“In addition, we found that the (shorter telomeres and high telomerase activity men) had blunted reactivity to acute stress in diastolic blood pressure, heart rate, and cortisol.”

No telomere-based differences occurred with women:

“The explanation for the sex difference in response profiles in our study is not clear. Hormonal processes are unlikely to be directly responsible, because women in this study were postmenopausal.”

http://www.pnas.org/content/111/12/4519.full “Shorter telomeres with high telomerase activity are associated with raised allostatic load and impoverished psychosocial resources”